Field of Invention
The present invention relates to the field of biotechnology, in particular to a RTN4B-related polypeptide, a monoclonal antibody thereof, a monoclonal antibody-producing hybridoma cell strain, and, preparation and applications thereof.
Description of Related Arts
RTN4B belongs to reticolon family (RTNs), and is named for containing special endoplasmic reticulum localization, and has conserved RHD structure frame (reticulon-homology domain). The family contains four genes of RTN1, RTN2, RTN3 and RTN4, wherein many reports are about researching RTN4. RTN4 (also named as Nogo/ASY/RTN-X) gene has a plurality of alternative splicing isoforms, which mainly encode three proteins of RTN4A (GenBank Accession number AF148537), RTN4B (GenBank Accession number AF148538), and RTN4C (GenBank Accession number AF087901), while some other alternative splicing isoforms are mainly specifically expressed in testis.
RTN4B shows ubiquitous expression in normal tissues, and studies found that RTN4B is closely related to the occurrence and development of a tumor. Firstly, RTN4B involves in the apoptotic regulation of tumor cells. Tsujimoto et al found that RTN4B enables to interact with Bcl-2 and Bcl-xL, and recruits Bcl-2 and Bcl-xL to the endoplasmic reticulum, to reverse the inhibition effect of apoptosis of Bcl-2 and Bcl-xL. Yutsudo et al found that RTN4B appears transcriptional repression in the sample of small cell lung cancer, while overexpression of RTN4B may significantly promote the apoptosis of tumor cells. Secondly, recent reports further found that RTN4B may well be related with vascular remodeling, and even angiogenesis. In 2004, Acevedo, L et al found that RTN4B shows expression in vascular endothelial cells and smooth muscle cells of a mammal RTN4B recombinant protein may promote the migration of vascular endothelial cells and inhibit the migration of smooth muscle cells. Next, RTN4A/B knockout mice appear abnormal thickening blood vessel walls and shrunken vascular lumen after vascular injury. Again, re-import RTN4B into mice through adenoviral vector, the abnormal thickening blood vessel walls can be restored to normal morphology. Therefore, RTN4B may well be the key molecule for mammals to maintain the morphology of blood vessel and to regulate reconstruction of blood vessel. Subsequently, the group further identified the receptor molecule of RTN4B on the endothelial cell surface, NgBR. The knock-down experiment has proved that the interaction between NogoB and NgBR is requisite for VEGF blood-derived molecule to induce angiogenesis. Miao et al have further proved that the interaction between NogoB and NgBR enables to regulate angiogenesis by activating the Akt pathway in cells.